It has been recognized for some time that inflammation in mammalian species can be traced at least in part to active oxygen species, including superoxide, and radicals associated therewith at the inflammatory site. Considerable research has been undertaken to measure and detect oxygen radicals, to establish the mechanisms whereby enzymes such as superoxide dismutase is effective in countering oxygen radical toxicity and even in the development and use of copper amine oxidases in preventing tissue damage and even in promoting damaged-tissue recovery.
However, the compounds which have been developed heretofore for active-oxygen or superoxide antagonism and destruction in vivo have not proved as effective as desired or were characterized by side reactions or could not be made in commercially significant quantities at reasonable cost.